Dietary pyridoxine potentiates thermal tolerance, heat shock protein and protect against cellular stress of Milkfish (Chanos chanos) under endosulfan-induced stress.

We herein report the protective role of pyridoxine in enhancing thermal tolerance of Milkfish Chanos chanos reared under endosulfan-induced stress. Four isocaloric and isonitrogenous diets were prepared with graded levels of pyridoxine (0, 50, 75 and 100 mg/kg). Two hundred and twenty five fishes were randomly distributed into four treatment groups in triplicate, reared under endosulfan-treated water, which were fed with pyridoxine supplemented diet, while the negative control group was reared without endosulfan-treatment and control fed. The concentration of endosulfan in treated water was maintained at a level of 1/40th of LC50 i.e. 0.52 µg/L. Dietary pyridoxine supplementation had significant (p < 0.01) effect on temperature tolerance viz. CTmax (Critical temperature maxima), LTmax (Lethal temperature maxima), CTmin (Critical temperature minima) and LTmin (Lethal temperature minima) of milkfish. The positive correlation was observed between CT max and LTmax (Y = -1.54 + 15.6x, R(2), 0.943) as well as CTmin and LTmin (Y = -1.44 + 1.021x, R(2), 0.941). At the end of the thermal tolerance study, antioxidative status and HSP 70 were significantly reduced in pyridoxine supplemented groups, whereas brain AChE was significantly (p < 0.01) elevated compared to positive and negative control. It is concluded that CTmax, LTmax, CTmin and LTmin, antioxidative status, neurotransmitter enzyme and HSP 70 strengthened the enhancement of thermal tolerance of Milkfish.

Acute toxicity, biochemical and histopathological responses of endosulfan in Chanos chanos.

This study investigated 96h median lethal concentration of endosulfan (99%, pure α: ß ratio of 7:3) by conducting static non-renewable acute toxicity bio-assay in Chanos chanos juvenile with average weight (110±5.65g). Further, the effect of different definitive doses (18.5, 19.5, 20.5, 21.5 and 22.5µg/L) of endosulfan on metabolic, heamato-immunoligcal and histopathological response were probed. Anti-oxidative enzymes CAT, SOD and GST showed significant (p<0.01) increase of activity in the liver, gill and brain during exposure to endosulfan in a dose and time dependent manner. The brain AChE activity showed significant (p<0.01) inhibition from 18.5 to 22.5µg/L exposure of endosulfan than the control group. LDH and MDH activity gradually increased with consequent increasing dose of endosulfan exposure in the liver, gill and brain. Similarly, ALT, AST and G6PDH activities in both liver and gill increased with consequent increases in the dose of endosulfan exposure. Immunological profile such as blood glucose and serum cortisol level significantly enhanced while respiratory burst activity declined with consequent increasing doses of endosulfan exposure. Histopathological alteration in the gill demonstrated curling of secondary lamellae, thickening of primary epithelium, shorting of secondary lamellae, epithelial hyperplasia, fusion of secondary lamellae, aneurism, and collapsed secondary lamellae due to dose dependent exposure of endosulfan. Liver histology illustrated cloudy swelling and necrosis with pyknotic nuclei to the moderate dose of endosulfan, whereas higher dose of endosulfan (21.5µg/L) displayed severe necrosis of hepatic cells. Overall results clearly indicate that acute exposure of endosulfan led to pronounced deleterious alterations on biochemical, heamato-immunological, and histopathological responses of C. chanos juvenile.

Dietary lecithin potentiates thermal tolerance and cellular stress protection of milk fish (Chanos Chanos) reared under low dose endosulfan-induced stress.

Endosulfan is an organochlorine pesticide commonly found in aquatic environments that has been found to reduce thermal tolerance of fish. Lipotropes such as the food additive, Lecithin has been shown to improve thermal tolerance in fish species. This study was conducted to evaluate the role of lipotropes (lecithin) for enhancing the thermal tolerance of Chanos chanos reared under sublethal low dose endosulfan-induced stress. Two hundred and twenty-five fish were distributed randomly into five treatments, each with three replicates. Four isocaloric and isonitrogenous diets were prepared with graded levels of lecithin: normal water and fed with control diet (En0/L0), endosulfan-treated water and fed with control diet (En/L0), endosulfan-treated water and fed with 1% (En/L1%), 1.5% (En/L 1.5%) and 2% (En/L 2%) lecithin supplemented feed. The endosulfan in treated water was maintained at the level of 1/40th of LC50 (0.52ppb). At the end of the five weeks, critical temperature maxima (CTmax), lethal temperature maxima (LTmax), critical temperature minima (CTmin) and lethal temperature minima (LTmin) were Determined. There was a significant (P<0.01) effect of dietary lecithin on temperature tolerance (CTmax, LTmax, CTmin and LTmin) of the groups fed with 1, 1.5 and 2% lecithin-supplemented diet compared to control and endosulfan-exposed groups. Positive correlations were observed between CT max and LTmax (R(2)=0.934) as well as between CTmin and LTmin (R(2)=0.9313). At the end of the thermal tolerance study, endosulfan-induced changes in cellular stress enzymes (Catalase, SOD and GST in liver and gill and neurotansmitter enzyme, brain AChE) were significantly (p<0.01) improved by dietary lecithin. We herein report the role of lecithin in enhancing the thermal tolerance and protection against cellular stress in fish exposed to an organochlorine pesticide.